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间歇性力诱导人牙周膜细胞中RANKL高表达。

Intermittent force induces high RANKL expression in human periodontal ligament cells.

作者信息

Nakao K, Goto T, Gunjigake K K, Konoo T, Kobayashi S, Yamaguchi K

机构信息

Division of Orofacial Functions and Orthodontics, Kyushu Dental College, Kitakyushu, Japan.

出版信息

J Dent Res. 2007 Jul;86(7):623-8. doi: 10.1177/154405910708600708.

Abstract

Intermittent compressive force stimulates bone resorption in orthodontic treatment. This study examined the molecular mechanism in human periodontal ligament (PDL) cells stimulated by an intermittent force. PDL cells were subjected to compressive force (2.0 or 5.0 g/cm(2)) for 2-4 days. Continuous or intermittent force was applied all day or for 8 hrs per day, respectively. At days 3 and 4, cell damage was less with intermittent force than with continuous force. At day 4, RANKL and IL-1beta expressions were greater with intermittent force than with continuous force. An IL-1 receptor antagonist inhibited the compressive force-induced RANKL expression. These findings indicate that IL-1beta is an autocrine factor regulating compressive force-induced RANKL expression in PDL cells, and that intermittent force can effectively induce RANKL in PDL cells with less cell damage.

摘要

间歇性压力在正畸治疗中会刺激骨吸收。本研究检测了间歇性压力刺激下人牙周膜(PDL)细胞的分子机制。对PDL细胞施加2.0或5.0 g/cm²的压力,持续2 - 4天。分别全天施加持续压力或每天施加8小时的间歇性压力。在第3天和第4天,间歇性压力造成的细胞损伤比持续压力小。在第4天,间歇性压力组的RANKL和IL - 1β表达高于持续压力组。IL - 1受体拮抗剂可抑制压力诱导的RANKL表达。这些发现表明,IL - 1β是调节PDL细胞中压力诱导RANKL表达的自分泌因子,且间歇性压力能在对细胞损伤较小的情况下有效诱导PDL细胞中的RANKL表达。

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